The most extensively studied members are Kv1.1 and Kv1.2, and mutations or autoimmune-mediated dysfunction of these channels result in a diverse range of neurological diseases including episodic ataxia, epilepsy, neuromyotonia, and myokymia (Paulhus et al., 2020; Ovsepian et al., 2016; Irani and Vincent, 2016). The gene discussed is KCNA2; the disease is Familial paroxysmal ataxia.